Methylglyoxal (MG) is considered by most cellular biologists to be a genotoxin; a substance toxic to genes and chromosomes and plays a critical role in disease and aging. It modifies residues of the amino acids arginine and lysine in proteins forming Advanced Glycation End-products (AGE's). MG irreversibly and progressively modify proteins, lipids and genes over time and is implicated in cellular mutagenesis, carcinogenesis, aging, blood vessel damage and leads to an inhibition of insulin signaling and the accelerated tissue damage characteristic of long-term complications of diabetes. (1) (2) (3) (5) (10) (11) (12). MG is also implicated in the cross-linking of collagen protein throughout the body in diabetics and the elderly which could partially explain the correlation between arterial stiffening and decreased joint mobility (13).

In cooked foods MG is formed by nonenzymic glycation or heat induced caramelization and subsequent millard reactions. Millard reaction is the browning reaction caused by external heat wherein a sugar and an amino acid form a complex that yield melanoidins and pigments; which are the strong flavor compounds and dark colors produced by browning foods.

MG is also formed spontaneously in living organisms from processed foods, fermented foods, and the consumption of foods stored for prolonged periods of time. (1) (4). Roasted coffee is one beverage that is high in MG due to the roasting of the beans and brewing at high temperatures; add sugar or flavored syrups or whipped cream and you compound the effect. Other foods and beverages high in MG include; beer, whisky and other liquor, soft drinks, toasted breads, cakes, cookies, pies, pastries, donuts, soy sauce. Manuka Honey was up to 1,000 fold higher in MG than regular honey and explains its cytotoxic effects against bacteria and why it is used as a wound dressing. (8) (11). In addition, cigarette smoking and passive smoke such as in cigars and pipes and smoke from hot oil cooking are all high in MG. (15) (16)

High protein diets such as the Atkins diet produces a state of ketosis and increases levels of by-products that are potential precursors of methylglyoxal. Ketotic subjects had and increase of 2.12 times methylglyoxal levels as compared to noncompliant, nonketotic subjects. (6). Prolonged fasting which also switches the body into ketosis produces high MG levels.

Surprisingly, vegetarians have a much higher blood concentration of MG than healthy omnivores. The theory is that vegetarians consume less proteins and thus less carnosine. The high sugar diet via fruit with predominance of fructose is higher in vegetarians. Higher fructose levels may cause an increase of AGE levels (19). in addition, many vegetarian diets are low caloric to the point of inducing a state of chronic, intermittent low-grade ketosis.

MG can deplete blood glutathione levels. In one study mice were exposed to MG via drinking water until two months of age. The result showed a marked decrease in blood glutathione activity and red blood cell capacity to counteract oxidative stress. The study results indicate that chronic intake of methylglyoxal, at levels that could be attained in food, is toxic by depletion of blood glutathione and could have adverse effect on some glutathione dependent functions in vivo. (7)

Protecting against methylglyoxal (MG) damage

Diet

An omnivore diet seems to be the best. High in vegetables, moderate in fruits. Berries are particularly beneficial due to lower in sugar content and high in antioxidants. Reduction in the consumption of high-heat cooked protein, carbohydrate and sugary foods where browning and charring is present. Roasting, charring, grilling, browning culinary treatments should be avoided. Avoid all packaged and processed foods and self-stable foods. Avoid sugary sodas and liquors.

Supplementation

In one study, Lipoic Acid significantly reduced the intracellular reactive oxygen species levels increased by MG. (9) Supplemental taurine showed a positive influence on collagen content from a high-fructose diet. (14) Carnosine has the potential to suppress many of the biochemical changes (e.g., protein oxidation, glycation, AGE formation, and cross-linking) that accompany aging and associated pathologies (17) (18).